It directly bound to PDE4D, restored cAMP signaling, suppressed MIF secretion in inflammatory fibroblasts, and disrupted fibroblast–dendritic cell interactions via the cAMP/protein kinase A (PKA)/cAMP‐response element binding protein (CREB) pathway, thereby significantly reducing the clinical and histological features of AD. The gene discussed is PDE4D; the disease is Alzheimer disease.